Embodiments of the present disclosure generally relate to methods and devices for anti-tachycardia pacing, and more particularly to delivery of anti-tachycardia pacing therapy by a low-power implantable medical device (IMD).
Ventricular tachycardia may be controlled through electrical therapy delivered by an implanted medical device, such as a pacemaker, implantable cardioverter defibrillator and the like. The device applies an electric stimulation to the heart muscle to interrupt or disrupt the fast rhythm. The electric stimulation may be in the form of timed pacemaker pulses or by high voltage shock. Anti-tachycardia pacing (ATP) has been used to convert a ventricular tachycardia into a normal sinus rhythm. Tachycardia is often the result of electrical feedback within the heart, wherein a natural beat results in the feedback of an electrical stimulus which prematurely triggers another beat. By interposing a stimulated heartbeat (i.e., a pacing pulse), the stability of the feedback loop is disrupted. For example, patients with monomorphic ventricular tachycardia (MVT) may be successfully paced out of the tachycardia using a rapid burst of high rate pacing. The burst includes a selected number of pulses that are delivered at the same rate, at an accelerating rate, or an alternating accelerating/decelerating rate.
Traditionally, ATP is delivered in bursts, where each burst includes a series of pulses. Several bursts may be given for any tachycardia episode. Following detection or redetection of a tachycardia, the first ATP pulse is delivered synchronously with an intrinsic event while the remaining pulses are delivered in a VOO mode.
Various approaches to ATP therapy have been utilized. For example, conventional ATP bursts may be delivered in accordance with one or more of ramping, scanning, adaptation, and/or a combination thereof. In convention ramped ATP, the ATP bursts are delivered with the interval between successive pulses shortened. In convention ATP scanning, each burst, that is used to treat a tachyarrhythmia event, may be delivered by progressively shortening the cycle length. When the burst cycle length is adjusting based on the intrinsic cycle length, the adjustment in the ATP therapy is called an adaptation. Typically ATP pulses have an amplitude of 7.5 V to 9.0V and have a pulse width of 1.0 to 1.5 ms. The pulses are delivered at intervals ranging from 200 to 550 milliseconds to provide 1.8 to 5 pulses per seconds.
However, conventional ATP therapies experience disadvantages when implemented by IMDs that utilize a low power source. For example, leadless pacemakers and other low power IMDs utilize batteries that are physically very small and exhibit a low initial charge. The leadless pacemakers and other low power IMDs experience a challenge to provide sustained voltages in excess of 6 V for a longer pulse widths (e.g., 0.4 ms) at a high pulse rate (e.g., 160 ppm or spaced at about 375 ms intervals). Instead, during delivery of conventional ATP therapy, the leadless pacemaker experiences a significant voltage drop when delivering ATP. As one example, if a leadless pacemaker utilized a battery that exhibits 1K ohms source impedance at some point in the life of the battery, the leadless pacemaker would experience approximately a 6% drop in pacing voltage (across the electrodes) when delivering a pacing pulse programmed to 6 V amplitude with a pulse width of 1.5 ms when delivering about 4 ATP pulses per second. Furthermore, if a 9 volt pacing pulse is programmed, a 10% drop in pacing amplitude would be expected. The drop in pacing voltage will be greater as the source impedance of the battery increases and battery source impedances for small batteries will increase well above 1 k over the battery's service life.
A need remains for an improved ATP therapy that does not require high rate pacing pulses to provide effective ATP and that affords an ATP therapy that is compatible with leadless pacemakers and other low power IMDs.